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Work capacity of the hypothermic heart
Annotations
Work
capacity
of the hypothermic
The term “work capacity” of the heart has been used in different ways and this has led to contradictory conclusions in regard to the ability of the hypethermic heart to perform external mechanical work.‘-3 Confusion has arisen chieflv from failure to distinguish between minute work-capacity, stroke work capacity, and total work capacity of an isolated heart. Conventionally, work capacity has been defined as the maximum external mechanical work which the heart is capable of performing per unit of time (usually a minute) without evidence of failure.4 To avoid confusion this may be called the “minute work capacity.” In this definition, one is uncertain whether the maximum cardiac work is attained by increments of cardiac output (volume load) or peripheral resistance (pressure load), or both. Since the heart can tolerate increments of volume load better than it does pressure load,& the maximum performance would vary with the type of work. Theoretically, there should be a certain combination of minute cardiac output and peripheral resistance that would give rise to the maximum minute work of the heart. Experimentally, however, it is not feasible to determine these “optimum” values. Hence, it is customary to use increments of volume work to estimate the minute work capacity of the heart.6 In the unanesthetized person or animal, no method is available at present for determining the minute work capacity of the healthy heart. The greatest load on the heart is observed during the severest muscular exercise, and it is generally held that the normal heart does not show signs of failure under these circumstances.? It should be noted that the minute work capacity of the intact heart cannot be a fixed value under different physiologic conditions. It would vary with neurogenic, hormonal, and other chemical influences acting on the heart. For instance, the minute capacity of the heart at rest would not be the same as in exercise (probably, it is much less). Methods are available for determining the minute work capacity of the heart in an anesthetized openchest animal. The technique of Sarnoff*ag appears to be most suitable, provided that the excessive increase in blood volume and arterial pressure is prevented. The simplest experimental setup for determining the minute work capacity of the heart is the denervated heart-lung preparation (HLP).e In such hearts the work capacity is much less than that of intact hearts, because of many factors, e.g., absence of
839
heart
positive chronotropic and inotropic actions of sympathetic nerves and adrenal hormones, biochemical changes in perfusing blood, limitation of output due to relatively narrow arterial cannula, regurgitation through atrioventricular valves due to lack of pericardial restraint, etc. In 1956, Reissmann and I&poor’ demonstrated that hypothermia down to 18°C. progressively reduced the minute work capacity of the dog heart in the HLP. Analysis of the data showed that this reduction was due entirely to the bradycardia of cold. The maximum stroke volume remained practically unchanged down to about 22°C. McMillan and associates2 have studied the stroke work capacity of the left ventricle in open-chest animals during hypothermia, and have observed that this capacity was not impaired by cooling to 28°C. Goldberg,lo and Covino and.Beaver+ measured ventricular contractile force by means of the straingauge arch and found an increase in the force of contraction, with peak values between 25” and 28°C. during hypothermia. Recently, Berne3 introduced another definition of “work capacity” which applies only to the isolated heart. In the rat heart-lung preparation, work capacity of the left ventricle was expressed as the product of mean arterial pressure and the total volume of blood pumped into the aorta (except the coronary flow) during an entire experiment. Since all such hearts are characterized by “spontaneous” failure, the cardiac output dropped progressively during an experiment. The arterial pressure was maintained constant (at an arbitrary level) by increasing the peripheral resistance periodically. Experiments were terminated when the heart could no longer pump enough blood to maintain the arterial pressure. Defined in this way, the “work capacity” of the hypothermic heart was noted to be much greater at 32” than at 3?“C.3J2 The introduction of this definition was unfortunate, in that it led to apparent contradiction in regard to the effect of cold on cardiac performance. Furthermore, this concept could not be applied to the intact or anesthetized animal. Actually, this method determines the total external work which an isolated heart is capable of performing while it is “spontaneously” failing as a result of its isolation. It is not unexpected that cold, which reduces the consumption of oxygen and increases the mechanical efficiency of the heart,‘s-ls should increase this capacity. Likewise, it is understandable that, in such experiments, reduced arterial pressure increased the
840
Am. Heart I. Jwze, 1962
Annotations
total work performance of the heart.‘2 In order to avoid confusion, we propose to designate this ability of the isolated heart as total work capacity. In summary, the following conclusions may be drawn in regard to the “work capacity” of the heart during hypothermia: Hypothermia progressively reduces the minute work capacity of the heart. This reduction is due to the bradycardia which occurs as a direct action of cold on the frequency of discharge of the pacemaker. The stroke work capacity of the heart is unchanged by cooling to 25”-28°C. Hypothermia improves myocardial contractility. The total work capacity of the isolated heart is increased by moderate hypothermia. This is related to the fact that isolated hearts fail spontaneously, and cold, by reducing the metabolic rate of the myocardium, delays the failure and increases the total work performance during the period of failure. In view of these different definitions of “work capacity” of the heart, it is recommended that the foregoing terminology be adopted to avoid contradictions that arise from semantics. From a clinical standpoint, the most important conclusion is that the hypothermic heart has a reduced minute work capacity and, hence, should not be overloaded, either as to outnut or arterial oressure. Henry S. Badeer, M.D. School of Medicine American University of Beirut Beirut, Lebanon REFERENCES Reissmann, K. R., and Kapoor, S.: Dynamics of hypothermic heart muscle (heart-lung preparation), Am. J. Physiol. 184:162, 1956. McMillan, I. K. R., Case, R. B., Stainsby, W. N., and Welch, G. H., Jr.: The hypothermic heart: work potential and coronary flow, Thorax 12:208, 1957. Berne, R. M.: Cardiodynamics and the coronary circulation in hypothermia, Ann. New York Acad. SC. 80:365, 1959. Katz, L. N.: Mechanism of heart failure, J. Mt. Sinai Hosp. 8:668, 1942.
Sarnoff, S. J., Braunwald, E., Welch, G. H., Jr., Case, R. B., Stainsby, W. N., and Macruz, R.: Hemodynamic determinants of oxygen consumption of the heart, with special reference to the tension-time index, Am. J. Physiol. 192:148, 1958. 6. Van Citters, R. L.: Work capacity of the left ventricle following ligation of the coronary arterv. AM. HEART T. 58:591. 1959. 7. Best,’ C. H., and Taylor, N. B.: The physiological basis of medical practice, ed. 6, Baltimore, 1955, The Williams & Wilkins Company, p. 255. 8. Sarnoff, S. J., and Berglund, E.: Ventricular function. I. Starling’s law of the heart studied by means of simultaneous right and left ventricular function curves in the dog, Circulation 9:706, 1954. 9. Sarnoff, S. J.: Myocardial contractility as described by ventricular function curves; observations on Starling’s law of the heart, Physiol. Rev. 35:107, 1955. 10. Goldberg, L. I.: Effects of hypothermia on contractility of the intact dog heart, Am. J. Physiol. 1%:92, 1958. 11. Covino, B. G., and Beavers, W. R.: Changes in cardiac contractility during immersion hypothermia, Am. J. Physiol. 195:433, 1958. 12. Savers. G.. and Solomon. N.: Work oerformante of a rat heart-lung preparation: standardization and influence of corticosteroids, Endocrinology 66:719, 1960. H.: Effect of hypothermia on oxygen 13. Badeer, consumption and energy utilization of heart, Circulation Res. 4:523, 1956. K. R., and Van Citters, R. L.: 14. Reissmann, Oxygen consumption and mechanical efficiency of the hypothermic heart, J. Appl. Physiol. 9:427, 1956. 15. Gerola, A., Feinberg, H., and Katz, L. N.: Myocardial oxygen consumption and coronary blood flow in hypothermia, Am. J. Physiol. 1%:719, 1959. 5.
,
Blood pressure and body build in men in tropical and temperate
In people of European descent who live in temperate climates, measurements of casual blood pressures have shown that the mean systolic and diastolic pressures rise with age, and that the mean systolic pressures rise quite steeply after the age of 5O.1-4 In people of non-European descent who live in tropical climates, the rise in mean pressures with age is smaller, and, in particular, there is no sharp rise after the age of SO.&-* Residence in a tropical climate might contribute to these differences, but the effect of climate can
,
Australia
only be assessed by comparing groups of people of the same race who lead similar lives, but who live in contrasted climates. Stevedores of European descent were studied in Cairns, Queensland (latitude 16” 55’S, average daily mean temperature of 76.3”F.) and Melbourne, Victoria (latitude 39’ 49/S., average daily mean temperature of 588°F.): The two population samples were well matched for age, occupation, living standards, height, weight, and arm circumference. The tropical group had more subcutaneous fat, as
Work
capacity
of the hypothermic
The term “work capacity” of the heart has been used in different ways and this has led to contradictory conclusions in regard to the ability of the hypethermic heart to perform external mechanical work.‘-3 Confusion has arisen chieflv from failure to distinguish between minute work-capacity, stroke work capacity, and total work capacity of an isolated heart. Conventionally, work capacity has been defined as the maximum external mechanical work which the heart is capable of performing per unit of time (usually a minute) without evidence of failure.4 To avoid confusion this may be called the “minute work capacity.” In this definition, one is uncertain whether the maximum cardiac work is attained by increments of cardiac output (volume load) or peripheral resistance (pressure load), or both. Since the heart can tolerate increments of volume load better than it does pressure load,& the maximum performance would vary with the type of work. Theoretically, there should be a certain combination of minute cardiac output and peripheral resistance that would give rise to the maximum minute work of the heart. Experimentally, however, it is not feasible to determine these “optimum” values. Hence, it is customary to use increments of volume work to estimate the minute work capacity of the heart.6 In the unanesthetized person or animal, no method is available at present for determining the minute work capacity of the healthy heart. The greatest load on the heart is observed during the severest muscular exercise, and it is generally held that the normal heart does not show signs of failure under these circumstances.? It should be noted that the minute work capacity of the intact heart cannot be a fixed value under different physiologic conditions. It would vary with neurogenic, hormonal, and other chemical influences acting on the heart. For instance, the minute capacity of the heart at rest would not be the same as in exercise (probably, it is much less). Methods are available for determining the minute work capacity of the heart in an anesthetized openchest animal. The technique of Sarnoff*ag appears to be most suitable, provided that the excessive increase in blood volume and arterial pressure is prevented. The simplest experimental setup for determining the minute work capacity of the heart is the denervated heart-lung preparation (HLP).e In such hearts the work capacity is much less than that of intact hearts, because of many factors, e.g., absence of
839
heart
positive chronotropic and inotropic actions of sympathetic nerves and adrenal hormones, biochemical changes in perfusing blood, limitation of output due to relatively narrow arterial cannula, regurgitation through atrioventricular valves due to lack of pericardial restraint, etc. In 1956, Reissmann and I&poor’ demonstrated that hypothermia down to 18°C. progressively reduced the minute work capacity of the dog heart in the HLP. Analysis of the data showed that this reduction was due entirely to the bradycardia of cold. The maximum stroke volume remained practically unchanged down to about 22°C. McMillan and associates2 have studied the stroke work capacity of the left ventricle in open-chest animals during hypothermia, and have observed that this capacity was not impaired by cooling to 28°C. Goldberg,lo and Covino and.Beaver+ measured ventricular contractile force by means of the straingauge arch and found an increase in the force of contraction, with peak values between 25” and 28°C. during hypothermia. Recently, Berne3 introduced another definition of “work capacity” which applies only to the isolated heart. In the rat heart-lung preparation, work capacity of the left ventricle was expressed as the product of mean arterial pressure and the total volume of blood pumped into the aorta (except the coronary flow) during an entire experiment. Since all such hearts are characterized by “spontaneous” failure, the cardiac output dropped progressively during an experiment. The arterial pressure was maintained constant (at an arbitrary level) by increasing the peripheral resistance periodically. Experiments were terminated when the heart could no longer pump enough blood to maintain the arterial pressure. Defined in this way, the “work capacity” of the hypothermic heart was noted to be much greater at 32” than at 3?“C.3J2 The introduction of this definition was unfortunate, in that it led to apparent contradiction in regard to the effect of cold on cardiac performance. Furthermore, this concept could not be applied to the intact or anesthetized animal. Actually, this method determines the total external work which an isolated heart is capable of performing while it is “spontaneously” failing as a result of its isolation. It is not unexpected that cold, which reduces the consumption of oxygen and increases the mechanical efficiency of the heart,‘s-ls should increase this capacity. Likewise, it is understandable that, in such experiments, reduced arterial pressure increased the
840
Am. Heart I. Jwze, 1962
Annotations
total work performance of the heart.‘2 In order to avoid confusion, we propose to designate this ability of the isolated heart as total work capacity. In summary, the following conclusions may be drawn in regard to the “work capacity” of the heart during hypothermia: Hypothermia progressively reduces the minute work capacity of the heart. This reduction is due to the bradycardia which occurs as a direct action of cold on the frequency of discharge of the pacemaker. The stroke work capacity of the heart is unchanged by cooling to 25”-28°C. Hypothermia improves myocardial contractility. The total work capacity of the isolated heart is increased by moderate hypothermia. This is related to the fact that isolated hearts fail spontaneously, and cold, by reducing the metabolic rate of the myocardium, delays the failure and increases the total work performance during the period of failure. In view of these different definitions of “work capacity” of the heart, it is recommended that the foregoing terminology be adopted to avoid contradictions that arise from semantics. From a clinical standpoint, the most important conclusion is that the hypothermic heart has a reduced minute work capacity and, hence, should not be overloaded, either as to outnut or arterial oressure. Henry S. Badeer, M.D. School of Medicine American University of Beirut Beirut, Lebanon REFERENCES Reissmann, K. R., and Kapoor, S.: Dynamics of hypothermic heart muscle (heart-lung preparation), Am. J. Physiol. 184:162, 1956. McMillan, I. K. R., Case, R. B., Stainsby, W. N., and Welch, G. H., Jr.: The hypothermic heart: work potential and coronary flow, Thorax 12:208, 1957. Berne, R. M.: Cardiodynamics and the coronary circulation in hypothermia, Ann. New York Acad. SC. 80:365, 1959. Katz, L. N.: Mechanism of heart failure, J. Mt. Sinai Hosp. 8:668, 1942.
Sarnoff, S. J., Braunwald, E., Welch, G. H., Jr., Case, R. B., Stainsby, W. N., and Macruz, R.: Hemodynamic determinants of oxygen consumption of the heart, with special reference to the tension-time index, Am. J. Physiol. 192:148, 1958. 6. Van Citters, R. L.: Work capacity of the left ventricle following ligation of the coronary arterv. AM. HEART T. 58:591. 1959. 7. Best,’ C. H., and Taylor, N. B.: The physiological basis of medical practice, ed. 6, Baltimore, 1955, The Williams & Wilkins Company, p. 255. 8. Sarnoff, S. J., and Berglund, E.: Ventricular function. I. Starling’s law of the heart studied by means of simultaneous right and left ventricular function curves in the dog, Circulation 9:706, 1954. 9. Sarnoff, S. J.: Myocardial contractility as described by ventricular function curves; observations on Starling’s law of the heart, Physiol. Rev. 35:107, 1955. 10. Goldberg, L. I.: Effects of hypothermia on contractility of the intact dog heart, Am. J. Physiol. 1%:92, 1958. 11. Covino, B. G., and Beavers, W. R.: Changes in cardiac contractility during immersion hypothermia, Am. J. Physiol. 195:433, 1958. 12. Savers. G.. and Solomon. N.: Work oerformante of a rat heart-lung preparation: standardization and influence of corticosteroids, Endocrinology 66:719, 1960. H.: Effect of hypothermia on oxygen 13. Badeer, consumption and energy utilization of heart, Circulation Res. 4:523, 1956. K. R., and Van Citters, R. L.: 14. Reissmann, Oxygen consumption and mechanical efficiency of the hypothermic heart, J. Appl. Physiol. 9:427, 1956. 15. Gerola, A., Feinberg, H., and Katz, L. N.: Myocardial oxygen consumption and coronary blood flow in hypothermia, Am. J. Physiol. 1%:719, 1959. 5.
,
Blood pressure and body build in men in tropical and temperate
In people of European descent who live in temperate climates, measurements of casual blood pressures have shown that the mean systolic and diastolic pressures rise with age, and that the mean systolic pressures rise quite steeply after the age of 5O.1-4 In people of non-European descent who live in tropical climates, the rise in mean pressures with age is smaller, and, in particular, there is no sharp rise after the age of SO.&-* Residence in a tropical climate might contribute to these differences, but the effect of climate can
,
Australia
only be assessed by comparing groups of people of the same race who lead similar lives, but who live in contrasted climates. Stevedores of European descent were studied in Cairns, Queensland (latitude 16” 55’S, average daily mean temperature of 76.3”F.) and Melbourne, Victoria (latitude 39’ 49/S., average daily mean temperature of 588°F.): The two population samples were well matched for age, occupation, living standards, height, weight, and arm circumference. The tropical group had more subcutaneous fat, as